Mold Exposure and Mitochondrial Antibodies

Luke Curtis, MD, MS; Allan Lieberman, MD, FAAEM

Context • Some studies have reported that airborne levels of mold above 150-1000 spores per cubic meter are sufficient to cause a wide range of human health problems. In trying to understand the mechanism of injury to the mitochondria that trigger an autoimmune response, researchers have learned that pyruvate carboxylase is a major site of antigenicity for antimitochondrial antibodies (AMA). Antibodies to mitochondria are found in over 90% of patients with primary biliary cirrhosis and are occasionally found in patients with other autoimmune diseases. Objectives • This study intended to examine the prevalence of antimitochondrial antibodies (AMA) in a population of patients exposed to molds, mycotoxins, and other toxins, Design • The research team described 6 case studies. Setting • The study occurred at an environmental- and occupational-medicine health clinic. Participants • Six patients at the clinic were the participants. These 6 patients represented 6.9% of a cohort of 87 patients who received autoimmune testing during that period. Outcome Measures • Participants received blood tests for autoimmune, metabolic, hormonal, and nutritional parameters, including AMA. Results • Six patients with a documented history of exposure to indoor mold, mycotoxin, and water damage had elevated levels of AMA. Conclusions • The fact that high levels of AMA in the 6 patients were all associated with mold and moisture exposure appears to be significant. Exposure to water- and mold-damaged indoor environments might damage mitochondria and trigger autoimmunity. Long term follow-up is needed to determine what may develop in these patients.

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